巨噬细胞炎症蛋白-1α在机械通气大鼠肺泡巨噬细胞中的表达

Expression of macrophage inflammatory protein-1α in alveolar macrophage in rat subjecting mechanical ventilation

目的通过检测不同潮气量机械通气大鼠肺泡巨噬细胞炎症蛋白-1α（macrophage inflammatory protein-1α，MIP—1α）和核因子κB（nuclear factor-kappa B，NF-κB）p65蛋白表达水平，探讨肺泡巨噬细胞（AM）活化在呼吸机所致肺损伤（VILI）中的作用。方法32只雄性Wistar大鼠随机分为对照组、小潮气量组、常规潮气量组和大潮气量组。采用SABC法分别测定各组大鼠BALF肺泡MIP-1α及NF-κB p65蛋白表达水平，并用100-CX型透射电镜观察其AM的超微结构。结果大潮气量和常规潮气量组大鼠BALF肺泡MIP-1α及NF-κB p65蛋白染色阳性细胞百分比均明显高于对照组和小潮气量组（P〈0．01）；大潮气量组大鼠BALF肺泡MIP—1α及NF-κB p65蛋白染色阳性细胞百分比与常规潮气量组比较亦有显著差异；小潮气量组与对照组比较差异无统计学意义（P〉0．05）。透射电镜下显示，大潮气量和常规潮气量组大鼠AM呈功能激活状态。结论AM是引起VILI的始动细胞之一，在VILI的发病中具有重要作用；AM活化并释放MIP-1α是引起肺内PMN聚集、活化，导致VILI发生的一个重要因素；AM表达与释放MIP-1α在某种程度上可能受NF-κB的调控。

Objective To explore the role of alveolar macrophage （AM） activation in ventilator induced lung injury（VILI） by measuring macrophage inflammatory protein-1α（MIP-1α） and nuclear factor- kappa B（NF-κB） p65 expressed in AM of rats with different tidal volume ventilations. Methods Thirty-two male Wistar rats were randomly divided into four groups：control group,low tidal volume group, conventional tidal volume group and high tidal volume group. The levels of MIP-1α and NF-κB p65 expressed in AM in BALF were measured by SABC method respectively and the ultrastructures of AM were observed with 100-CX transmission electron microscope. Results The percentages of AM in BALF stained positively with MIP-1α and NF-κB p65 both in high and conventional tidal volume groups were significantly higher than those in control and low tidal volume groups （ P 〈0.01）. The percentages of AM in BALF stained positively with MIP-1α and NF-κB p65 in high tidal volume group were also significantly higher than those in conventional tidal volume group （ P 〈0.05）,but no statistical differences existed between low tidal volume group and control group. Under transmission electron microscope the AM in high and conventional tidal volume groups appeared in active state. Conclusions AM is one of the starting cells to inducing VILI and plays an important role in VILI. AM activation and releasing MIP-1α is one of the main reasons leading to neutrophils aggregated and activated in the lungs and so to developing VILI. AM expression and releasing MIP-1α may be regulated by NF-κB to some extent.